Predominant acetylcholine-induced vasoconstriction in isolated, perfused simian facial veins.

Using the cannula insertion method, we investigated the vascular response to acetylcholine (ACh) and other vasoactive substances. ACh consistently induced only vasoconstriction, whereas isoproterenol and norepinephrine usually induced dilatation. Vasoconstriction induced by phenylephrine was less potent than that induced by ACh. Clonidine and xylazine did not induce significant vascular responses. ACh-induced constrictions were readily inhibited by atropine and slightly potentiated by physostigmine. They were slightly but significantly inhibited by pirenzepine (a muscarinic M1-receptor antagonist), but not influenced by AF-DX 116 (a M2-receptor antagonist). 4-DAMP (4-diphenylacetoxy N-methylpiperidine; a M3-receptor antagonist), strongly inhibited the ACh-induced constrictions. They were not modified by bunazosin but slightly suppressed by diltiazem. Removal of the endothelium did not significantly modify the ACh-induced constrictions. From our results, we conclude that the simian facial vein has many constrictory muscarinic receptors, especially of the M3 subtype.